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[Committee_on_Risk_Assessment_of_Exposure_to_Radon] Risk Assessment of Radon in Drinking Water

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[Committee_on_Risk_Assessment_of_Exposure_to_Radon] Risk Assessment of Radon in Drinking Water

[Committee_on_Risk_Assessment_of_Exposure_to_Radon] Risk Assessment of Radon in Drinking Water

Risk Assessment of Radon in

Drinking Water

Committee on Risk Assessment of Exposure to Radon in Drinking Water
Board on Radiation Effects Research
Commission on Life Sciences
National Research Council

Washington, D.C. 1999

NATIONAL ACADEMY PRESS • 2101 Constitution Avenue, NW • Washington, D.C. 20418

NOTICE: The project that is the subject of this report was approved by the
Governing Board of the National Research Council, whose members are drawn
from the councils of the National Academy of Sciences, the National Academy of
Engineering, and the Institute of Medicine. The members of the committee
responsible for the report were chosen for their special competences and with
regard to appropriate balance.

This report was prepared under EPA Contract EPA X825492-01-0 between
the National Academy of Sciences and the Environmental Protection Agency.

Library of Congress Cataloging-in-Publication Data

Risk assessment of radon in drinking water / Committee on Risk

Assessment of Exposure to Radon in Drinking Water, Board on

Radiation Effects Research, Commission on Life Sciences, National

Research Council.

p. cm.

Includes bibliographical references and index.

ISBN 0-309-06292-6 (casebound).

1. Drinking water—Contamination—United States. 2. Radon—Health

aspects. 3. Indoor air pollution—Health aspects—United States. 4.

Radon mitigation. 5. Health risk assessment—United States. I.

National Research Council (U.S.). Committee on Risk Assessment

of Exposure to Radon in Drinking Water.

RA592.A1 R57 1999 99-6134


Risk Assessment of Radon in Drinking Water is available for sale from the
National Academy Press, 2101 Constitution Avenue, N.W., Box 285, Washing-
ton, DC 20055; 1-800-624-6242 or 202-334-3313 (in the Washington metro-
politan area); Internet,

Copyright1999 by the National Academy of Sciences. All rights reserved.

Printed in the United States of America


JOHN DOULL (Chair), University of Kansas Medical Center, Kansas City, KS
THOMAS B. BORAK, Colorado State University, Fort Collins, CO
JAMES E. CLEAVER, Department of Dermatology, University of California,

San Francisco, CA
KEITH F. ECKERMAN, Oak Ridge National Laboratory, Oak Ridge, TN
LINDA C.S. GUNDERSEN, US Geological Survey, Reston, VA
NAOMI H. HARLEY, New York University School of Medicine, New York,

CHARLES T. HESS, University of Maine, Orono, ME
PHILIP K. HOPKE, Clarkson University, Potsdam, NY
NANCY E. KINNER, University of New Hampshire, Durham, NH
KENNETH J. KOPECKY, Fred Hutchinson Cancer Research Center, Seattle,

THOMAS E. McKONE, University of California, Berkeley, CA
RICHARD G. SEXTRO, Lawrence Berkeley National Laboratory, Berkeley,



JONATHAN M. SAMET, Johns Hopkins University, Baltimore, MD


STEVEN L. SIMON, Study Director, Board on Radiation Effects Research
KAREN M. BRYANT, Project Assistant
DORIS E. TAYLOR, Staff Assistant


NANCY CHIU, US Environmental Protection Agency



JOHN B. LITTLE (Chair), Harvard School of Public Health, Boston, MA
R.J. MICHAEL FRY, Oak Ridge, TN*
S. JAMES ADELSTEIN, Harvard Medical School, Boston, MA†‡
VALERIE BERAL, University of Oxford, United Kingdom
EDWARD R. EPP, Harvard University, Boston, MA†
HELEN B. EVANS, Case Western Reserve University, Cleveland, OH†
MERRIL EISENBUD, Chapel Hill, NC (deceased August 1997)
MAURICE S. FOX, Massachusetts Institute of Technology, Cambridge, MA§
PHILIP C. HANAWALT, Stanford University, Palo Alto, CA (member until

LYNN W. JELINSKI, Cornell University, Ithaca, NY
WILLIAM F. MORGAN, University of California, San Francisco†
WILLIAM J. SCHULL, The University of Texas Health Science Center,

Houston, TX
DANIEL O. STRAM, University of Southern California, Los Angeles, CA
SUSAN W. WALLACE, University of Vermont, Burlington, VT
H. RODNEY WITHERS, UCLA Medical Center, Los Angeles, CA


EVAN B. DOUPLE, Director, Board on Radiation Effects Research
RICK JOSTES, Senior Program Officer
STEVEN L. SIMON, Senior Program Officer
CATHERINE S. BERKLEY, Administrative Associate
KAREN BRYANT, Project Assistant
PEGGY JOHNSON, Project Assistant
DORIS E. TAYLOR, Staff Assistant

*New BRER Chair effective 7/1/98
†New members effective 7/1/98



THOMAS D. POLLARD (Chair), The Salk Institute for Biological Studies, La
Jolla, CA

FREDERICK R. ANDERSON, Cadwalader, Wickersham & Taft, Washington,

JOHN C. BAILAR, III, University of Chicago, IL
PAUL BERG, Stanford University School of Medicine, Palo Alto, CA
JOANNA BURGER, Rutgers University, Piscataway, NJ
SHARON L. DUNWOODY, University of Wisconsin, Madison, WI
JOHN L. EMMERSON, Indianapolis, IN
NEAL L. FIRST, University of Wisconsin, Madison, WI
URSULA W. GOODENOUGH, Washington University, St. Louis, MO
HENRY W. HEIKKINEN, University of Northern Colorado, Greeley, CO
HANS J. KENDE, Michigan State University, East Lansing, MI
CYNTHIA J. KENYON, University of California, San Francisco, CA
DAVID M. LIVINGSTON, Dana-Farber Cancer Institute, Boston, MA
THOMAS E. LOVEJOY, Smithsonian Institution, Washington, DC
DONALD R. MATTISON, University of Pittsburgh, Pittsburgh, PA
JOSEPH E. MURRAY, Wellesley Hills, MA
EDWARD E. PENHOET, Chiron Corporation, Emeryville, CA
MALCOLM C. PIKE, Norris/USC Comprehensive Cancer Center, Los

Angeles, CA
JONATHAN M. SAMET, The Johns Hopkins University, Baltimore, MD
CHARLES F. STEVENS, The Salk Institute for Biological Studies, La Jolla,

JOHN L. VANDEBERG, Southwest Foundation for Biomedical Research, San

Antonio, TX


PAUL GILMAN, Executive Director
ALVIN G. LAZEN, Associate Executive Director


The National Academy of Sciences is a private, nonprofit, self-perpetuating
society of distinguished scholars engaged in scientific and engineering research,
dedicated to the furtherance of science and technology and to their use for the
general welfare. Upon the authority of the charter granted to it by the Congress in
1863, the Academy has a mandate that requires it to advise the federal govern-
ment on scientific and technical matters. Dr. Bruce M. Alberts is president of the
National Academy of Sciences.

The National Academy of Engineering was established in 1964, under the
charter of the National Academy of Sciences, as a parallel organization of out-
standing engineers. It is autonomous in its administration and in the selection of
its members, sharing with the National Academy of Sciences the responsibility
for advising the federal government. The National Academy of Engineering also
sponsors engineering programs aimed at meeting national needs, encourages
education and research, and recognizes the superior achievements of engineers.
Dr. William A. Wulf is the president of the National Academy of Engineering.

The Institute of Medicine was established in 1970 by the National Academy
of Sciences to secure the services of eminent members of appropriate professions
in the examination of policy matters pertaining to the health of the public. The
Institute acts under the responsibility given to the National Academy of Sciences
by its congressional charter to be an adviser to the federal government and, upon
its own initiative, to identify issues of medical care, research, and education. Dr.
Kenneth I. Shine is president of the Institute of Medicine.

The National Research Council was organized by the National Academy of
Sciences in 1916 to associate the broad community of science and technology
with the Academy’s purposes of furthering knowledge and advising the federal
government. Functioning in accordance with general policies determined by the
Academy, the Council has become the principal operating agency of both the
National Academy of Sciences and the National Academy of Engineering in
providing services to the government, the public, and the scientific and engineer-
ing communities. The Council is administered jointly by both Academies and the
Institute of Medicine. Dr. Bruce M. Alberts and Dr. William A. Wulf are chair-
man and vice chairman, respectively, of the National Research Council.



At the request of the Environmental Protection Agency (EPA) pursuant to a
congressional mandate (amendment to bill S. 1316 to amend title XIV of the
Public Health Service Act commonly known as the Safe Drinking Water Act), the
National Research Council has appointed a multidisciplinary committee to con-
duct a study and report on the health risks associated with exposure to radon in
drinking water. The committee was also asked to prepare an assessment of the
health-risk reduction associated with various mitigation measures to reduce ra-
don in indoor air; to accomplish this task, the committee used the results of the
latest scientific studies of risk assessment and relevant peer-reviewed research
carried out by organizations and individual investigators. Finally, the committee
was asked to summarize the agreements and differences between the various
advisory organizations on the issues relevant to the health risks posed by radon in
drinking water and radon-mitigation measures and to evaluate the technical and
scientific bases of any differences that exist.

The Committee on Risk Assessment of Radon in Drinking Water was ap-
pointed in May 1997, held its first meeting on July 14-15, 1997, and held six
additional meetings during the next 9 months. The ability of the committee to
comply with this extremely tight schedule is a reflection of the dedication and
expertise of the committee members and the efforts of the committee staff.

The committee acknowledges the help of those individuals or organizations
who gave presentations during our meetings and/or provided information in re-
sponse to requests by committee members or staff and to others who helped the
committee in the completion of our task.



Gustav Akerbloom, Swedish Radiation Protection Institute
Hannu Arvela, Finnish Radiation/Nuclear Safety Authority
Timothy Barry, Environmental Protection Agency
David S. Chase, New Hampshire Radiologic Health Bureau
Gail Charnley, Presidential/Congressional Commission on Risk Assessment

and Risk Management
Nancy Chiu, Environmental Protection Agency
Jack Correia, Massachusetts General Hospital
Bill Diamond, Environmental Protection Agency
Joe Drago, Kennedy Jenks, San Francisco, CA
Susumo Ito, Professor Emeritus, Harvard University
Dan Krewski, Environmental Health Centre, Ottawa, Canada
Jay Lubin, National Cancer Institute
J.P. Malley, Jr., University of New Hampshire
Sylvia Malm, Environmental Protection Agency
Frank Marcinowski, Environmental Protection Agency
Lars Mjones, Swedish Radiation Protection Institute
Roger McClellan, Chemical Industry Institute of Toxicology
Neal S. Nelson, Environmental Protection Agency
David Paris, Waterworks, Manchester, NH
Dan Pederson, American Water Works Association
Frederick Pontius, American Water Works Association
Jerome Puskin, Environmental Protection Agency
Edith Robbins, New York University
David Rowson, Environmental Protection Agency
Richard Toohey, Oak Ridge Institute of Science and Education
George Sachs, VA Medical Center, Los Angeles
Anita Schmidt, Environmental Protection Agency
Daniel J. Steck, St. John’s University
Grant Stemmerman, University of Cincinnati
Neil Weinstein, Rutgers University
Jeanette Wiltse, Environmental Protection Agency

This report has been reviewed by individuals chosen for their diverse per-
spectives and technical expertise, in accordance with procedures approved by the
National Research Council’s Report Review Committee. The purpose of this
independent review is to provide candid and critical comments that will assist the
authors and the National Research Council in making their published report as
sound as possible and to ensure that the report meets institutional standards for
objectivity, evidence, and responsiveness to the study charge. The content of the
review comments and draft manuscript remain confidential to protect the integ-
rity of the deliberative process. We wish to thank the following individuals for
their participation in the review of this report:


Antone Brooks, Washington State University, Tri-Cities
Bernard Cohen, University of Pittsburgh
Douglas Crawford-Brown, University of North Carolina-Chapel Hill
Robert E. Forster, The University of Pennsylvania School of Medicine
Sharon Friedman, Lehigh University
Patricia L. Gardner, New Jersey Department of Environmental Protection
Roger O. McClellan, Chemical Industry Institute of Toxicology
Gilbert Omenn, University of Washington
Frank H. Stillinger, Bell Laboratories
Rhodes Trussell, Montgomery Watson, Inc.

The committee members would like to express their gratitude to the staff of
the National Research Council’s Board on Radiation Effects Research. The com-
mittee members are especially appreciative for study director Steven Simon’s
technical guidance and encouragement. They are also grateful to Karen Bryant
and Doris Taylor for assistance with administrative details related to the com-
mittee’s work.



The Origin of Radon, 23
Absorbed Dose from Indoor Radon, 27 50
Composition of the Report, 31
Indoor Radon, 32
Radon in Groundwater and Public Water Supplies, 36
Ambient Radon, 37

Measurements of Transfer Coefficients, 51
Modeling of Transfer Coefficient, 52
Conclusions, 57

Intakes and Consumption of Water, 59
Physicochemical Properties of Radon, 60
Fate of Radon Decay Products in the Body, 73



Cancer Risk Per Unit 222Rn Concentration in Drinking Water, 76
Special Populations at Risk, 81



Inhalation of Radon and Its Short-lived Decay Products, 82
Risk Posed by Inhalation of 222Rn Decay Products, 82
Lung Dose from 222Rn Gas, 83
Dose to Organs Other Than the Lung from Inhaled 222Rn, 84
222Rn Decay-Product Dose During Showering, 84
Lung-Cancer Risk Posed by Inhalation of 222Rn Decay Products, 93

Epidemiology of Childhood Exposure and Lung-Cancer Risk, 100

Environmental and Domestic Epidemiology, 100

Epidemiology of Cancer of Organs Other Than Lung, 102
Evaluation of Risk Per Unit Exposure from Inhaled 222Rn in Air, 103



Cells at Risk, 105

Cellular Damage Induced by Radon Alpha Particles, 107

Transformation of Cells by Alpha Particles in Vitro, 110

DNA Damage and Its Repair—the Caretaker Genes, 110

Deletion Mutagenesis and Chromosomal Changes Caused by Densely

Ionizing Radiation, 114

Control of Cellular Responses to Damage—the Arbitrator Gene, 115

Apoptosis—the Undertaker Genes, 116

Initial Genetic Changes in Carcinogenesis—the Gatekeeper Genes, 118

Tumor Growth and Nutrition—the Caterers, 119

Genetic Instability in Irradiated Cell Populations—the Diversifiers, 120

Mutations in α-Particle-Induced Tumors—the Fingerprints, 121

Epidemiologic, Biophysical, and Cell-Based Models of Radon-Induced

Carcinogenesis, 122

Reliability of a Health-Risk Assessment, 126
Environmental Protection Agency Process for Assessing and Evaluating
Uncertainties in Radon Risk, 127
Issues in Uncertainty Analysis for Radon, 129
The Committee’s Evaluation of Uncertainties in Risk Assessment of
Radon in Drinking Water, 130
Communication of Uncertain Risk Information, 137
Discussion and Recommendations, 139


Mitigation of Radon in Indoor Air, 141
Mitigation of Radon in Water, 160
Conclusions, 179


Derivation of the Alternative Maximum Contaminant Level (AMCL), 181

Equivalent Risk-Reduction Scenarios, 182

Scenario 1: High Radon Concentrations in Water, 183

Scenarios 2-4: Effects of Distribution of Radon in Indoor Air, 184

Scenario 5: Use of New Radon-Resistant Construction, 187

Scenario 6: Multicommunity Mitigation, 188

Scenario 7: Use of Outreach, Education, and Incentives, 189

Scenario 8: Outreach for Other Health Risks, 193

Equity and Implementation Issues and Risk Reduction, 193

Summary, 196




A Behavior of Radon and Its Decay Products in the Body 241
B A Model for Diffusion of Radon Through the Stomach Wall 249
C Water-Mitigation Techiques
D Risks Associated with Disinfection By-products Formed by Water 254

Chlorination Related to Trihalomethanes (THMs) 257
E Gamma Radiation Dose from Granular-Activated Carbon (GAC) 260

Water Treatment Units
F EPA Approach to Analyzing Uncertainty and Variability


Public Summary

Radiation is a natural part of the environment in which we live. All people
receive exposure from naturally occurring radioactivity in soil, water, air and
food. The largest fraction of the natural radiation exposure we receive comes
from a radioactive gas, radon. Radon is emitted from uranium, a naturally occur-
ring mineral in rocks and soil; thus, radon is present virtually everywhere on the
earth, but particularly over land. Thus, low levels of radon are present in all the
air we breathe. There are three forms of radon, but the use of the term radon in
this report refers specifically to radon-222. Although it cannot be detected by a
person’s senses, radon and its radioactive by-products are a health concern be-
cause they can cause lung cancer when inhaled over many years. A recent report
by the National Research Council suggested that between 3,000 and 32,000 lung-
cancer deaths each year (the most likely value is given as 19,000 deaths) in the
United States are associated with breathing radon and its radioactive by-products
in indoor air, but these deaths are mainly among people who also smoke.

Most of the radon that enters a building comes directly from soil that is in
contact with or beneath the basement or foundation. Radon is also found in well
water and will enter a home whenever this water is used. In many situations such
as showering, washing clothes, and flushing toilets, radon is released from the
water and mixes with the indoor air. Thus, radon from water contributes to the
total inhalation risk associated with radon in indoor air. In addition to this, drink-
ing water contains dissolved radon and the radiation emitted by radon and its
radioactive decay products exposes sensitive cells in the stomach as well as other
organs once it is absorbed into the bloodstream. This report examines to what
degree this ingested radon is a health risk and to what extent radon released



from water into air increases the health risk due to radon already in the air in

Approximately half of the drinking water in the United States comes from
ground water that is tapped by wells. Underground, this water often moves
through rock containing natural uranium that releases radon to the water. Water
from wells normally has much higher concentrations of radon than does surface
water such as lakes and streams.

Radon concentrations can be measured either in terms of a volume of air
(becquerel of radon per cubic meter) or a volume of water (becquerel of radon per
liter). The average concentration of radon in public water supplies derived from
ground water sources is about 20 becquerel per liter (540 pCi). Some wells have
been identified with high concentrations, up to 400 times the average. Surface
water, such as in lakes and streams, has the lowest concentrations, about one-
tenth that of most wells.

Drinking-water quality in the United States is regulated by the Environmen-
tal Protection Agency (EPA) under the Safe Drinking Water Act (SDWA). Since
radon is acknowledged as a cancer-causing substance, the law directs EPA to set
a maximum contaminant level (MCL) for radon to restrict the exposure of the
public to the extent that is possible, that is, as close to zero as is feasible.

In 1991, EPA proposed an MCL for radon of 11 becquerel per liter (about
300 pCi per liter) for radon in drinking water. In 2000, the agency is required to
set a new MCL based in part on this report. The law also directed EPA to set an
alternative MCL (AMCL); an AMCL is the concentration of radon in water that
would cause an increase of radon in indoor air that is no greater than the level of
radon naturally present in outdoor air. Limiting public risk from radon by treating
the water alone is not feasible because radon is also naturally present in the air.
Thus, the AMCL is the tool that allows EPA to limit exposure to radon in water
to a practical level, that is, allowing no more risk from the radon in water than is
posed by the level of radon naturally present in outdoor air.

The 1996 amendments to the Safe Drinking Water Act required EPA to fund
the National Academy of Sciences (NAS) to determine the risk from radon in
drinking water and also to determine the public-health benefits of various meth-
ods of removing radon from indoor air.

In response to that agreement, the NAS established through its principal
operating agency, the National Research Council, a committee which has evalu-
ated various issues related to the risk from radon in drinking water and provides
here the information needed by EPA to set the AMCL. The primary conclusion
from the committee’s investigation into the risk of inhaling radon as compared to
drinking water containing dissolved radon is as follows:

Most of the cancer risk resulting from radon in the household water supply is
due to inhalation of the radioactive by-products that are produced from radon
that has been released from the water into the air, rather than from drinking the
water. (The risk from radon is higher among smokers because the combination


of radon and smoke has a greater damaging effect than the sum of the individual
risks.) Furthermore, the increased level of indoor radon that is caused by using
water in the home is generally small compared with the level of indoor radon
that originated in the soil beneath the home.

Based on an analysis of the available data on radon concentrations outdoors
and on the transfer from water to air, the Research Council committee arrived at
these additional conclusions:

• The average outdoor air concentration over the entire United States is

about 15 becquerel per cubic meter (405 pCi per cubic meter or 0.4 pCi per liter).

• The contribution to radon concentration in indoor air from household

usage of water is very low—only about one ten-thousandth the water concentra-
tion. The reason the resulting airborne concentration is so low is because only
about half of the radon in the household water supply escapes into the air and then
it is diluted into the large volume of air inside the home.

• Combining this information, the committee has determined that the level

of radon in drinking water that would cause an increase of radon in indoor air that
is no greater than the level of radon naturally present in outdoor air is about 150
becquerel per liter (4,050 pCi per liter). This conclusion will affect the public and
water utilities in the following ways:

1. People who own their own wells are not legally obliged to do anything
because the Safe Drinking Water Act does not regulate private wells. How-
ever, people who are served by private wells and who wish to minimize their
risk should test their water and consider taking action to reduce the radon if
the concentration in the water is above the AMCL. In addition, those people
should also measure the indoor air concentration in their home and consider
taking actions to reduce it if it is above EPA’s recommended action levels.
Lastly, as the earlier NRC report concluded, stopping smoking is the most
effective way to reduce the risk of lung cancer and reduce the risks associated
with radon.

2. Water supplies serving 25 or more people or with 15 or more connections
are considered to be public water supplies. Those supplies, along with some
special cases such as schools, will be subject to radon regulation if they rely on
groundwater. In this case, there are three possibilities: (a) The radon in the water
is already below the MCL. This will apply to the majority of people in the United
States—only about 1 of every 14 individuals routinely consumes water with
concentrations greater than the 1991 proposed MCL (11 becquerel per liter or
300 pCi/L). For water below the MCL, nothing needs be done. (b) The radon in
the water is greater than the AMCL. In this case, radon reduction (mitigation)
would be required by law after the regulation is final. Data available to the
committee indicate that there are several types of water mitigation technology
that could effectively reduce the radon concentration to the MCL. (c) The radon
in the water is between the MCL and the AMCL. In this case, the concentration


must be reduced to the MCL or, if there is an approved state plan, the risk to the
population served by the water supply can be reduced by activities that reduce
radon in air and/or water.

The committee discussed a variety of methods to reduce radon entry into
homes and the concentrations in the indoor air and in water. Ventilation systems
can be used to reduce radon concentrations in indoor air to acceptable levels.
Periodic testing would be needed to ensure the continued successful operation of
individual air treatment systems. New homes can be constructed using methods
to reduce airborne radon (radon resistant construction). However, there is not
enough evidence at the present time to be certain these techniques are effective.
Several water-treatment technologies to remove radon from water are very effec-
tive, however, they do not address the largest risk to the occupants of the house,
namely radon in air.

The EPA mandate is to reduce public risk caused by exposure to radon. For
those communities where the public water supply contains radon at concentra-
tions between the MCL and the AMCL, the law will allow individual states to
reduce the risk to their population through multimedia measures to mitigate radon
levels in indoor air. A state may develop and submit a multimedia program to
mitigate radon levels in indoor air for approval by the EPA Administrator. The
Administrator shall approve a state program if the health risk reduction benefits
expected to be achieved by the program are equal to or greater than the health risk
reduction benefits that would be achieved if each public water system in the state
complied with the MCL. If the program is approved, public water systems in the
state may comply with the alternative maximum contaminant level in lieu of the
MCL. State programs may rely on a variety of mitigation measures, including
public education, home radon testing, training, technical assistance, remediation
grant and loan or other financial incentive programs, or other regulatory or
nonregulatory measures. As required by SDWA, EPA is developing guidelines
for multimedia mitigation programs. If there is no approved state multimedia
mitigation program, any public water system in the state may submit a program
for approval by the EPA Administrator, according to the same criteria, conditions
and approval process that would apply to a state program. In this scenario, water
utilities can minimize the level of risk to their consumers—even if the water they
provide is higher than the MCL (but lower than the AMCL)—by reducing air-
borne radon in some of the community’s homes. Because the risk caused by
inhaled radon is so much greater than that caused by radon that is swallowed in
water, reducing the airborne radon in only a few homes may reduce public risk
enough for the water utility to be in compliance with the multimedia program

With regard to multimedia programs, the committee’s report provides dis-
cussion of risk-reduction methods at the community level and of ways to evaluate
the effectiveness of reducing radon-related risk within a community or region


served by a water utility. One risk reduction technique is public education pro-
grams to encourage radon mitigation from indoor air. The previously conducted
education and outreach programs reviewed by the committee were largely unsuc-
cessful; therefore, the committee concluded that public education and outreach
programs alone would be insufficient to achieve a measurable reduction in health

A multimedia mitigation program will reduce radon risks in indoor air in lieu
of reduction to the MCL in drinking water. The specific design of each commu-
nity water utility’s program will depend on many factors. At the same time,
complicated risk-reduction programs like those discussed here have many poten-
tial difficulties. For example, for water utilities that provide water that contains
radon at levels between the MCL and the AMCL, the feasibility of using a
multimedia mitigation program will depend on whether there are homes with
relatively high indoor radon concentrations. Only in those homes is it feasible to
reduce the air concentration sufficiently such that an expensive, large-scale water
mitigation program in the region is not needed to satisfy the multimedia program
requirements. The key issue is determining how many buildings must have air
mitigation systems to obtain a reduction in public risk equal to that which could
be achieved by reducing radon in the water supplied to the community. More-
over, air monitoring programs will be needed to identify the homes whose indoor
air must be mitigated and effective outreach programs will be needed to educate
the public about the need to modify these homes to reduce indoor radon so that
the water utility can demonstrate the risk reduction needed for compliance. Fi-
nally, consideration needs to be given to how the costs of mitigation of private
homes will be apportioned among homeowners and the water utilities or state

Another potential problem is the present-day scarcity of trained personnel
(particularly in the water utilities) that could design or maintain home air mitiga-
tion systems and carry out the tests needed to ensure continued performance of
these systems.

Finally, the committee recognizes that the reduction in risk by multimedia
programs will not be distributed equally among the public. The mitigation of
indoor-air radon in a small number of homes means risk reduction among only a
few people who had high initial risk, rather than a uniform risk reduction for a
whole population served by the water utility.

The various analyses conducted allowed the committee to estimate the risk
and annual number of fatalities caused by radon in water and to compare it with
the risk caused by radon in air. The figure presented here summarizes the cancer
risk posed by inhaling radon in air (with and without the addition of radon from
using water in the home) and the risk posed by drinking water that contains
dissolved radon. Specifically, in 1998 in the United States, there will be about
160,000 deaths from lung cancer, mainly as a result of smoking tobacco. Of
those, about 19,000 are estimated to result from inhaling radon gas in the home;


though most of these deaths will be among people who smoke. Of the 19,000
deaths, only 160 are estimated to result from inhaling radon that was emitted
from water used in the home though most of these deaths would also among
smokers. As a benchmark for comparison, about 700 lung-cancer deaths each
year can be attributed to exposure to natural levels of radon while people are

The committee determined that the risk of stomach cancer caused by drink-
ing water that contains dissolved radon is extremely small and would probably
result in about 20 deaths annually compared with the 13,000 deaths from stomach
cancer that arises from other causes.

Except in situations where concentrations of radon in water are very high,
reducing the radon in water will generally not make a large difference in the total
radon-related health risks to occupants of dwellings. Using techniques to reduce
airborne radon and its related lung-cancer risk makes good sense from a public-
health perspective. However, there are concerns about the equity of the multime-
dia approach.

The committee concludes that evaluating whether a multimedia approach to
radon reduction will achieve an acceptable risk reduction in a cost-effective and
equitable manner will be a complex process. It will require significant coopera-
tion among EPA, state agencies, water utilities and local governments, especially
because many of the communities affected by the radon regulation will be very
small and they will need assistance in making decisions concerning the advan-
tages or disadvantages of a multimedia program. Thus, each public water supply
will find it necessary to study its own circumstances carefully before deciding to
undertake a multimedia mitigation program instead of treating the water to re-
duce the radon dissolved in it.



Executive Summary

Of all the radioisotopes that contribute to natural background radiation, ra-
don presents the largest risk to human health. There are three naturally occurring
isotopes of radon, but the use of the term radon in this report refers specifically to
222Rn, which is a decay product of 238U. A recent report by the National Research
Council suggested that between 3,000 and 32,000 lung-cancer deaths annually
(the most likely value for the number of deaths is 19,000) in the United States are
associated with exposure to 222Rn and its short-lived decay products in indoor air,
largely because radon substantially increases the lung-cancer risk for smokers.
Most radon enters homes via migration of soil gas. Throughout this report,
radon activity concentrations are cited in the SI1 unit of becquerel per cubic meter
(Bq m–3; 1 Bq m–3 = 0.027 pCi L–1). The mean annual radon concentration
measured in the living areas of homes in the United States is 46 Bq m–3.
Radon has also been identified as a public-health concern when present in
drinking water. Surface waters contain a low concentration of dissolved radon.
Typically radon concentrations in surface waters are less than 4,000 Bq m–3.2
Water from ground water systems can have relatively high levels of dissolved
radon, however. Concentrations of 10,000,000 Bq m–3 or more are known to exist
in public water supplies. Many of the water supplies containing substantial con-
centrations of radon serve very small communities (<1,000 people). Data on

1 International System of Units (SI) adopted in 1960 by the 11th General Conference on Weights
and Measurements (see for example NIST 1995; NIST 1991).

2 Note that 1 cubic meter (m3) is equivalent in volume to 1,000 L. Thus, 4,000 Bq m–3 is equiva-
lent to 4 Bq L–1.



radon in water from public water supplies indicate that elevated concentrations of
radon in water occur primarily in the New England states, the Appalachian states,
the Rocky Mountain states, and small areas of the Southwest and the Great

Because radon is easily released by agitation in water, many uses of water
release radon into the indoor air, which contributes to the total indoor airborne
radon concentration. Ingestion of radon in water is also thought to pose a direct
health risk through irradiation of sensitive cells in the gastrointestinal tract and in
other organs once it is absorbed into the bloodstream. Thus, radon in drinking
water could potentially produce adverse health effects in addition to lung cancer.

Drinking-water quality in the United States is regulated by the Environmen-
tal Protection Agency (EPA) under the Safe Drinking Water Act originally passed
in 1974. In the 1986 amendments to the act, EPA was specifically directed to
promulgate a standard for radon as one of several radionuclides to be regulated in
drinking water. Because of delays in implementing the regulation of radionu-
clides in drinking water, EPA was sued. In a consent decree, EPA agreed to
publish final rules for radionuclides in drinking water, including radon, by April

EPA proposed national primary drinking water regulations for radionuclides
in 1991. Because radon is a known carcinogen, its maximum contaminant level
goal (MCLG) was automatically set at zero. A maximum contaminant level
(MCL) of 11,000 Bq m–3 was subsequently proposed as the level protective of
public health and feasible to implement taking costs into account. Public com-
ments on the proposed regulations suggested that the MCL for radon be set
somewhere from less than 1,000 Bq m–3 to 740,000 Bq m–3; a large majority
favored setting the MCL at value higher than 11,000 Bq m–3.

In 1992, Congress directed the Office of Technology Assessment to analyze
the EPA health risk assessment and outline actions that could address regulation
of radon, considering both air and water. Also in 1992, the Chaffee-Lautenberg
amendment to the EPA appropriation bill for FY 1993 directed the agency to seek
an extension of the deadline for publishing a final rule until October 1993 and to
submit a report, reviewed by EPA’s Science Advisory Board (SAB), to Congress
by July 1993. That report was to address the risks posed by human exposure to
radon and consider both air and water sources, the costs of controlling or mitigat-
ing exposure to waterborne radon, and the risks posed by treating water to re-
move radon. The SAB review of the report questioned EPA’s estimates of the
number of community water supplies affected, the extrapolation of the risk of
lung cancer associated with the high radon exposures of uranium miners to the
low levels of exposure experienced in domestic environments and the magnitude
of risk associated with ingestion. The SAB report also emphasized that the risk of
cancer from radon in domestic settings was a multimedia issue and that the risk
for radon in water must be considered within the context of the total risk from
radon, which is dominated by radon in indoor air. The Office of Management and


Budget also expressed concern about EPA’s analysis of the cost of mitigation. In
the agency’s FY 1994 appropriation bill, Congress ordered EPA to delay publish-
ing a rule for radon in drinking water.

The 1996 amendments to the Safe Drinking Water Act required EPA to
contract with the National Academy of Sciences (NAS) to conduct a risk assess-
ment of radon in drinking water and an assessment of the health-risk reduction
benefits associated with various measures to reduce radon concentrations in in-
door air. EPA is also required to publish an analysis of the health-risk reduction
and the costs associated with compliance with any specific MCL before issuing a
proposed regulation. The law also directed EPA to promulgate an alternative
maximum contaminant level (AMCL) if the proposed MCL is less than the con-
centration of radon in water “necessary to reduce the contribution of radon in
indoor air from drinking water to a concentration that is equivalent to the national
average concentration of radon in outdoor air.” Under the law, states may de-
velop a multimedia mitigation progam which if approved by EPA would allow
utilities whose water has radon concentrations higher than the MCL, but lower
than the AMCL, to comply with the AMCL. The multimedia programs to miti-
gate radon in indoor air may include “public education; testing; training; techni-
cal assistance; remediation grants, loan or incentive programs; or other regulatory
or non-regulatory measures.” If a state does not have an EPA-approved multime-
dia mitigation program, a public water supply in that state may submit such a
program to EPA directly. Public water supplies exceeding the AMCL and choos-
ing to institute a multimedia mitigation program to achieve equivalent health risk
reductions must, at a minimum, treat their water to reduce radon in water concen-
trations to less than or equal to the AMCL. The present report was written to
address the issues just discussed.


It has been difficult to set a standard for radon, as opposed to other radionu-
clides in drinking water, because of the absence of authoritative dosimetric infor-
mation for radon dissolved in water. Furthermore, radon presents a unique regu-
latory problem in that its efficient transfer from water into indoor air produces a
risk from the inhalation of its decay products. Thus, it is regulated as a radionu-
clide in water, but a major portion of the associated risk occurs because of its
contribution to the airborne radon concentration.

Because of the relatively small volume of water used in homes, the large
volume of air into which the radon is emitted, and the exchange of indoor air with
the ambient atmosphere, radon in water typically adds only a small increment
to the indoor air concentration. Specifically, radon at a given concentration in
water adds only about 1/10,000 as much to the air concentration; that is, typical
use of water containing radon at 10,000 Bq m–3 will on average increase the air
radon concentration by only 1 Bq m–3. There is always radon in indoor air


from the penetration of soil gas into homes, so only very high concentrations
of radon in water will make an important contribution to the airborne

Even though water generally makes only a small contribution to the indoor
airborne radon concentration, the risk posed by radon released from water, even
at typical groundwater concentrations, is estimated to be larger than the risks
posed by the other drinking water contaminants that have been subjected to
regulation, such as disinfection by-products. Thus, in most homes, the risk to the
occupants posed by indoor radon is dominated by the radon from soil gas, which
is not subject to regulation, and a change in the radon in drinking water would
produce a minimal change in the risk posed by airborne radon. This problem led
to the suggestion that mitigation of radon in indoor air be considered an alterna-
tive means of achieving risk reduction equal to or greater than that which would
be achieved by reducing the concentration of radon in drinking water.

The ingestion of radon in water also presents a possible risk. Questions were
raised with respect to the ingestion risk assessment that EPA used in the 1991
proposed regulations and in the revised multimedia risk assessment of 1994. The
questions were related to the applicability of some of the data used as the basis of
the risk model and to the resulting assumptions that were used to estimate risk.
The substantial uncertainties in the radon health risks other than those posed by
inhalation add to the problems of setting an appropriate MCL to protect public
health. Thus, a reevaluation of the ingestion risks was needed.


EPA contracted with NAS to address the issues cited above, and the commit-
tee on the Risk Assessment of Radon Gas in Drinking Water was formed in the
National Research Council’s Board on Radiation Effects Research. The specific
tasks assigned to the committee were:

• To examine the development of radon risk assessments for both inhala-

tion and ingestion of water.

• To modify an existing risk model if that was deemed appropriate or to

develop a new one if not.

• To review the scientific data and technical methods used to arrive at risk

coefficients for radon in water.

• To assess potential health-risk reduction benefits associated with various

mitigation measures to reduce radon in indoor air.

The final report includes:

• Estimates of cancer risk per unit activity concentration of radon in water.
• Assessment of the state of knowledge with respect to health effects of


radon in drinking water for populations at risk, such as infants, children, pregnant
women, smokers, elderly persons, and seriously ill persons.

• Review of information regarding teratogenic and reproductive effects in

men and women due to radon in water.

• Estimates of the transfer coefficient relating radon in water to average

radon concentrations in indoor air.

• Estimates of average radon concentrations in ambient air.
• Estimates of increased health risks that could result from methods used to

comply with regulations for radon in drinking water.

• Discussion of health-risk reduction benefits obtained by reducing radon

using currently available methods developed for reducing radon concentrations
in indoor air and comparison of these benefits with those achievable by the
comparable reduction of risks associated with mitigation of radon in water.


The committee’s report addresses each of those points, and its conclusions
are summarized below. The order of presentation below follows that in the report.

Occurrence of Radon in the United States

National data on indoor radon, radon in water, and geologic radon potential
indicate systematic differences in the distribution of radon across the United
States. Geologic radon-potential maps and statistical modeling of indoor radon
exposures make it clear that the northern United States, the Appalachian and
Rocky Mountain states, and states in the glaciated portions of the Great Plains
tend to have higher than average indoor radon concentrations. Some smaller
areas of the southern states also have higher than average indoor radon concentra-
tions. Data on radon in water from public water supplies indicate that elevated
concentrations of radon in water occur in the New England states, the Appala-
chian states, the Rocky Mountain states, and small areas of the Southwest and the
Great Plains.

National Average Ambient Radon Concentration

The ambient concentration of radon varies with distance from and height
over its principal source in the ground (rocks and soil) and from other sources that
can locally or regionally affect it, such as lakes, mine or mill tailings, vegetation,
and fossil-fuel combustion. However, diurnal fluctuations due to changes in air
stability and meteorologic events account for most of the variability. Average
ambient radon concentrations were measured by EPA over nine seasons at 50
sites across the United States. Most, but not all, sites coincided with the capital
city of the state but did not statistically represent the population across the U.S.,


nor were the measurement at these sites necessarily representative of average
ambient radon concentrations in each state. But the EPA data set is the only one
with a fully national extent. The committee does not believe that the data are
sufficiently representative to provide a population-weighted annual average am-
bient radon concentration. An unweighted arithmetic mean radon concentra-
tion of 15 Bq m–3, with a standard error of 0.3 Bq m–3 was calculated based
on the EPA data set, and the committee recommends use of this value as the
best available national ambient average concentration. After reviewing all the
other ambient radon concentration data that are available from other specific
sites, the committee concluded that the national average ambient radon concen-
tration would lie between 14 and 16 Bq m–3.

Transfer Coefficient

The transfer coefficient is the average fraction of the initial average radon
concentration in water that is contributed to the indoor airborne radon concentra-
tion. The average transfer coefficient estimated by a model and the average
estimated from measurement data are in reasonable agreement. The average of
the measurements was 0.9 × 10–4 with a standard error of 0.1 × 10–4, and the
model’s average was either 0.9 × 10–4 or 1.2 × 10–4 depending on the choice of
input parameter values. Having considered the problems with both the mea-
surements of the transfer coefficient and the measurements that are the
input values into the model, the committee concludes that the transfer coef-
ficient is between 0.8 ؋ 10–4 and 1.2 ؋ 10–4 and recommends that EPA
continue to use 1.0 ؋ 10–4 as the best central estimate of the transfer coeffi-
cient that can now be obtained.

Biologic Basis of Risk Estimation

The biologic effects of radon exposure under the low exposure conditions
found in domestic environments are postulated to be initiated by the passage of
single alpha particles with very high linear energy transfer. The alpha-particle
tracks produce multiple sites of DNA damage that result in deletions and rear-
rangements of chromosomal regions and lead to the genetic instabilities impli-
cated in tumor progression. Because low exposure conditions involve cells ex-
posed to single tracks, variations in exposure translate into variations in the
number of exposed cells, rather than in the amount of damage per cell. This
mechanistic interpretation is consistent with a linear, no-threshold relation-
ship between high-linear energy transfer (high-LET) radiation exposure and
cancer risk, as was adopted by the BEIR VI committee. However, quantita-
tive estimation of cancer risk requires assumptions about the probability of
an exposed cell becoming transformed and the latent period before malig-
nant transformation is complete. When these values are known for singly hit


cells, the results might lead to reconsideration of the linear no-threshold
assumption used at present.

Ingestion Risk

The cancer risk arising from ingestion of radon dissolved in water must be
derived from calculations of the dose absorbed by the tissues at risk because no
studies have quantified the risk. Studies of the behavior of radon and other inert
gases have established that they are absorbed from the gastrointestinal tract and
readily eliminated from the body through the lungs. The stomach, the portal of
entry of ingested radon into the body, is of particular concern. The range of alpha
particles emitted by radon and its short-lived decay products is such that alpha
particles emitted within the stomach are unable to reach the cells at risk in the
stomach wall. Thus, the dose to the wall depends heavily on the extent to which
radon diffuses from the contents into the wall. Once radon has entered the blood,
through either the stomach or the small intestine, it is distributed among the
organs according to the blood flow to them and the relative solubility of radon in
the organs and in blood. Radon dissolved in blood that enters the lung will
equilibrate with air in the gas-exchange region and be removed from the body.

The committee found it necessary to formulate new mathematical models of
the diffusion of radon in the stomach and the behavior of radon dissolved in blood
and other tissues. The need for that effort arose from the lack of directly appli-
cable experimental observations and from limitations in the extent to which one
can interpret available studies. The diffusion of radon within the stomach was
modeled to determine the expected time-integrated concentration of radon at the
depth of the cells at risk. The result, based on a diffusion coefficient of 5 ×
10–6 cm2 s–1, indicated that a conservative estimate of the integrated concentra-
tion in the wall was about 30% of that in the stomach content.

The committee also found it useful to set forth a physiologically-based phar-
macokinetic (PBPK) model of the behavior of radon in the body. Various inves-
tigators have assessed the retention of inhaled and ingested radon in the body, but
their observations do not relate directly to the distribution of radon among the
tissues. The PBPK is formulated using information on blood flow to the tissues
and on the relative solubility of radon in blood and tissue to determine the major
tissue of deposition (which was adipose tissue) and retention within this tissue.
The PBPK model is consistent with the observations regarding radon behavior in
the body. Unlike previous estimates of the radiation dose, the committee’s analy-
sis also considered that each radioactive decay product formed from radon decay
in the body exhibited its own behavior with respect to tissues of deposition,
retention, and routes of excretion.

The committee’s estimates of cancer risk are based on calculations with risk-
projection models for specific cancer sites. The computational method was that
described in EPA’s Federal Guidance Report 13. An age- and gender-averaged


cancer death risk from lifetime ingestion of radon dissolved in drinking water
at a concentration of 1 Bq m–3 is 0.2 ؋ 10–8. Stomach cancer is the major contribu-
tor to the risk. The actual risk from ingested radon could be as low as zero depend-
ing on the validity of the linear, no-threshold dose response hypothesis, however,
the committee has estimated confidence limits on the ingestion risk (see chapter 4).

Inhalation Risk

Lung cancer arising from exposure to radon and its decay products is bron-
chogenic. The alpha-particle dose delivered to the target cells in the bronchial
epithelium is necessarily modeled on the basis of physical and biologic factors.
The dose depends particularly on the diameter of the inhaled ambient aerosol
particles to which most of the decay products attach. These particles deposit on
the airway surfaces and deliver the pertinent dose, and the dose can vary, because
of changes in particle size, by about a factor of 2 in normal home conditions.

The dose from radon gas itself is smaller than the dose from decay products
on the airways, mainly because of the location of the gas in the airway relative to
the target cells—that is, the source-to-target geometry. The dose from radon gas
that is soluble in body tissues is also smaller than the decay-product dose. Two of
the underground-miner studies showed no statistically significant risk of cancer
in organs other than the lung due to inhaled radon and radon decay products. The
dosimetry supports that observation, although there is a need to continue the
miner observations.

The risk of lung cancer associated with lifetime inhalation of radon in air at
a concentration of 1 Bq m–3 was estimated on the basis of studies of underground
miners. The values were based on risk projections from three follow-up studies:
BEIR IV (National Research Council 1988), NIH (1994) and BEIR VI (National
Research Council 1999). These three reports used data from 4 to 11 cohorts of
underground miners in seven countries and developed risk projections of 1.0 ×
10–4, 1.2 × 10–4, and 1.3 × 10–4 per unit concentration in air (1 Bq m–3), respec-
tively. The three values were for a mixed population of smokers and nonsmokers.
The value adopted by the committee is the rounded average derived from
the two BEIR-VI model results and equals 1.6 ؋ 10–4 per Bq m–3. The lung-
cancer risk to smokers is statistically significantly higher than the risk to non-
smokers. Given the adopted transfer coefficient of 1 ؋ 10–4, the risk of lung
cancer (discussed in two reports of the National Research Council and one of
the National Institutes of Health) posed by lifetime exposure to radon (222Rn)
in water at 1 Bq m–3 was calculated to be 1.6 ؋ 10–8.

Summary of Risk Estimates

The risk estimates developed by the committee for radon in drinking water
are summarized in table ES-1. Although the committee was asked to estimate the


risks to susceptible populations—such as infants, children, pregnant women,
smokers, and elderly and seriously ill persons—there is insufficient scientific
information to permit such estimation except for the lung-cancer risk to smokers,
which is presented separately in the table. The adopted lifetime risk of lung
cancer for a mixed population of smokers and nonsmokers, men and women,
resulting from the air exposure to radon from a waterborne radon concen-
tration of 1 Bq m–3 is 1.6 ؋ 10–8. The adopted lifetime risk of stomach cancer
for the same water concentration is 0.2 ؋ 10–8; the committee could not
make a distinction in ingestion risk for any specifically identified subpopula-
tion other than the differences in gender.

Figure 1 (see Public Summary) puts the inhalation and ingestion risks into
perspective by direct comparison of annual cancer deaths. The number of lung-
cancer deaths in the United States is estimated to be 160,100 in 1998 (ACS 1998).
Using the average of the two BEIR-VI risk models and adjusting for the 1998
increase in the number of lung-cancer deaths, the committee estimates there will
be about 19,000 lung-cancer deaths in 1998 attributable to radon and the combi-
nation of radon and smoking. The committee estimated there might be about 20
stomach-cancer deaths in 1998 (with a subjectively determined uncertainty range
from 1 to 50 deaths) attributable to the ingestion of radon in drinking water as
compared to 13,700 stomach-cancer deaths that are estimated to develop in the
United States in 1998 from all causes (ACS 1998). Based on an estimated na-
tional mean value of radon in drinking water, the committee estimates 160 lung
cancer deaths in 1998 (with a subjectively determined range from 25 to 280
deaths) attributable to indoor radon (in air) resulting from the release of radon
from household water. The committee’s analysis indicates that most of the
cancer risk posed by radon in drinking water arises from the transfer of
radon into indoor air and the subsequent inhalation of the radon decay
products, and not from the ingestion of the water.

TABLE ES-1 Committee Estimate of Lifetime Risk Posed by Exposure to
Radon in Drinking Water at 1 Bq m–3

Exposure Pathway Lifetime risk Female U.S. Populationa

Inhalation (ever-smokers)b Male 2.0 × 10–8 2.6 × 10–8
Inhalation (never-smokers)b 0.4 × 10–8 0.50 × 10–8
Inhalation (population)b 3.1 × 10–8 1.2 × 10–8 1.6 × 10–8
Ingestion 0.59 × 10–8 0.23 × 10–8 0.19 × 10–8
2.1 × 10–8
0.15 × 10–8

Total Risk (inhalation and ingestion) 2.2 × 10–8 1.4 × 10–8 1.8 × 10–8

aThese rounded values combine the various subpopulations, with appropriate weighting factors taken
from the 1990 U.S. Census.
bBased on the radon decay product risks of BEIR VI Report (National Research Council 1999) and
includes the incremental dose to showering with the uncertainties in these estimates.


The committee was asked to review teratogenic and reproductive risks. There
is no scientific evidence of teratogenic and reproductive risks associated with
radon in tissues from either inhalation or ingestion.

Comparison of the Present Analysis with the Previous EPA Analyses

The committee’s analysis results in a modest reduction of the overall risk
associated with radon in drinking water compared with the two previous analyses
conducted by the EPA. However, the magnitudes of the risks associated with the
different exposure pathways are different, as shown in table ES-2. The com-
mittee’s analysis estimates that the inhalation pathway accounts for about
89% of the estimated cancer risk and ingestion accounts for 11%. In con-
trast, EPA’s 1994 analysis suggested that inhalation accounted for 47% of
the overall risk and ingestion accounted for 53%.

Based on the committee’s analysis, the estimated inhalation risk has increased
while the estimated ingestion risk has decreased. The committee did not do any new
analysis for the inhalation risk. An average risk value based on three studies: BEIR
IV, NIH, and BEIR VI (NRC 1988; Lubin et al. 1994; NRC 1999; respectively)
was adopted. The committee did conduct a new analysis of the ingestion risk, based
on a model developed for this study. This model reduces the overall ingestion risk
factor by about a factor of 5, and suggests that, in contrast with the previous EPA
analysis, almost all of the ingestion risk is attributed to the stomach. The estimated
ingestion risk factors for various organs are compared in table ES-2.

There are a number of factors underlying the analysis of the risk associated
with radon in drinking water, in addition to the lifetime radiation risk factors
described above. These include the amount of water ingested, the effective expo-

TABLE ES-2 Comparison of Individual Lifetime Risk Estimates Posed by
Radon in Drinking Water at a Concentration of 1 Bq m–3

Exposure Pathway Committee 1991 EPA 1994 Revised EPA
Analysisa Proposed Ruleb Analysisc
(A) Radon progeny inhalationa
(B) Radon inhalation 1.6 × 10–8 1.3 × 10–8 0.81 × 10–8
(C) Ingestion 0.05 × 10–8 0.054 × 10–8
0.2 × 10–8 0.4 × 10–8 0.95 × 10–8
Colon 1.6 × 10–9 2.0 × 10–9 4.9 × 10–9
Liver 0.059 × 10–9 0.46 × 10–9 1.4 × 10–9
Lung 0.058 × 10–9 0.33 × 10–9 0.25 × 10–9
General tissue 0.034 × 10–9 0.55 × 10–9 1.2 × 10–9
0.079 × 10–9 0.61 × 10–9 1.5 × 10–9
Total risk (A+B+C)
1.8 × 10–8 1.8 × 10–8 1.8 × 10–8

aTotal for the U.S. population (averaging across sex and smoking status).
bEPA 1991b.
cEPA 1994b.


sure duration and the overall water-to-air transfer factor. The EPA reanalysis (EPA
1994b) used a direct tapwater consumption rate of 1 L d–1, an exposure time of
70 y, and assumed that 20% of the radon in the tapwater is released from the water
in the process of transferring the water from the tap to the stomach (tapwater is
defined as water ingested directly, without agitation or heating). The committee
used an age- and gender-specific tapwater usage rate that corresponds to an age-
and gender-average rate of 0.6 L d–1 and assumed all of the radon remained dis-
solved in the water during the transfer process. Both the EPA and the committee
analyses used a transfer factor of 1 × 10–4 for purposes of estimating the contribu-
tion radon dissolved in water makes to the overall indoor air radon concentration.

The estimated number of cancer deaths per year from public exposure to
radon are compared in table ES-3. Ranges estimated by this committee are ap-
proximate and are based on judgment using the best available information.

Uncertainty Analysis

Estimating potential human exposures to and health effects of radon in drink-
ing water involves the use of large amounts of data and the use of models for
projecting relationships outside the range of observed data. The data and models
must be used to characterize population behaviors, engineered-system perfor-
mance, contaminant transport, human contact, and dose-response relationships
among populations in different areas, so large variabilities and uncertainties are
associated with the resulting risk characterization. The report provides an evalu-
ation of the importance of and methods for addressing the uncertainty and vari-
ability that arise in the process of assessing multiple-route exposures to and the
health risks associated with radon.

TABLE ES-3 Comparison of estimated cancer deaths per year due to
exposure to radon and estimated possible ranges due to uncertainty

Exposure Pathway Committee Revised EPA
Inhalation of radon progeny in indoor air Analysisa Analysisc
Inhalation of radon progeny in outdoor air 18,200b
(3,000-33,000) 520
Inhalation of radon progeny derived from 720
the release of radon from drinking water (120-1300) 86
Ingestion of radon in drinking water (25-290)d 100

aBased on the 1998 estimated U.S. population of 270 million.
bBased on data from BEIR VI (National Research Council 1999).
cBased on a U.S. population of 250 million (EPA 1994b).
dValues derived from rescaling the analysis of the EPA-SAB (1994b) report using 1998 population

and mortality data and risk estimates from BEIR VI (National Research Council 1999).


The data, scenarios, and models used to represent human exposures to radon
in drinking water include at least four important relationships (i) The magnitude
of the source-medium concentration, that is, the concentrations of radon in the
water supply and in other relevant media, such as ambient air, (ii) the contami-
nant concentration ratio, which defines how much a source-medium concentra-
tion changes as a result of transfers, transformation, partitioning, dilution, and so
on before human contact, (iii) the extent of human contact, which describes
(often on a body-weight basis) the frequency (days per year) and magnitude
(liters per day) of human contact with a potentially contaminated exposure me-
dium (tap water, indoor air, or outdoor air), and (iv) the likelihood of a health
effect, such as cancer, associated with a predicted extent of human contact. The
latter area of uncertainty includes that of the dose-response model assumed.
Uncertainties in modeling the movement of radon with the wall of the stomach
(model structure), in the model parameters, and the lack of relevant experimental
observations are the critical sources of uncertainty. The key points discussed
included one overarching issue, that being how uncertainty and variability
can affect the reliability of the estimates of health effects for any exposure
scenario and related control strategies.

Mitigation of Radon in Air

There has been considerable research on and practical experience with the
use of active (mechanical) systems for the control of radon entry into buildings.
Use of such systems, when they are properly installed and operating, can typi-
cally yield indoor airborne radon concentrations below 150 Bq m–3 and can often
result in concentrations of about 75 Bq m–3. Although there is considerable
experience with the design and installation of active systems, monitoring pro-
grams are needed to ensure the continued successful operation of individual
active systems. Another possible way to reduce risks associated with exposure to
airborne radon is to design and build radon-resistant new buildings. Although the
technical potential for building radon-resistant buildings has been demonstrated
under some circumstances, the scientific basis for ensuring that it can be done
reliably and as a consistent outcome of normal design and construction methods
is inadequate. With the exception of the results in research conducted in
Florida, there are no comparative data on which to base estimates of the
overall effects of radon-resistant construction methods on reducing concen-
trations of radon in indoor air radon concentrations.

Mitigation of Radon in Water

Several water treatment technologies have been used to effectively remove
radon from water. However various issues and secondary effects must be ad-
dressed in connection with each method, including intermedia pollution (transfer


of radon from water to air) in the case of aeration and the retention of radionu-
clides (gamma-ray exposure and waste disposal) in the case granular activated
carbon (GAC) adsorption. If water must be treated to meet either the AMCL or
the MCL, disinfection might be required to meet the pending groundwater rule.
In this case, the risk associated with the disinfection byproducts, as estimated by
the committee, will be smaller than the risk reduction gained from radon removal.
The committee has estimated the equivalent gamma dose from a GAC system
designed to remove radon from a public water supply. The dose depends heavily
on the details and geometry of the system and should be predicted with an
extended-source model that can be modified to simulate the actual dimensions of
the treatment units.

Multimedia Approach to Risk Reduction

The 1996 Safe Drinking Water Act Amendments permit EPA to establish an
alternative maximum contamination level (AMCL) if the MCL is low enough so
that the contribution of waterborne radon to the indoor radon concentration is less
than the national average concentration in ambient air. The AMCL is defined
such that the waterborne contribution of radon to the indoor air concentration is
equal to the radon concentration in outdoor air, which is taken to be the national
average ambient radon concentration. In the situations where radon concentra-
tions in water are greater than the MCL but less than the AMCL, states or water
utilities can develop a multi-media approach to health risk reduction. The EPA is
required to publish guidelines including criteria for multimedia approaches to
mitigate radon in indoor air that result in a reduction in risk to the population
living in the area served by a public water supply that contains radon in concen-
trations greater than the MCL. The committee has examined some of the imple-
mentation issues involved in a multimedia mitigation approach through a se-
quence of scenarios that explore the possible options.

The MCL will be determined by EPA based on a variety of considerations
including their risk assessment, measurement technology, and best available
treatment options and thus, a specific value has not yet been determined. The
ratio of the average ambient radon air concentration to the transfer coefficient
defines the AMCL. On the basis of the committee’s recommended values
for the average ambient radon concentration and the average transfer
coefficient, the AMCL would be 150,000 Bq m–3 (about 4,000 pCi L–1).
Water in excess of the AMCL must be mitigated at least to the AMCL, and
alternative means can then be used to provide a health-risk reduction equivalent
to what would be obtained by mitigation of the water to the MCL. However,
because of the relatively small cost difference between mitigating the water to
the AMCL and to the MCL, the committee believes that in most cases multime-
dia mitigation programs will probably not be considered for public water sup-
plies with water concentrations in excess of the AMCL. For high radon concen-


tration water, it will generally be most cost-effective to mitigate radon in water
to the MCL.

For water supplies with radon concentrations between the MCL and the
AMCL, the feasibility of implementing a multimedia mitigation program
depends on the availability of homes in which the airborne radon concentra-
tion is high (greater than 150 Bq m–3). EPA has divided the country into three
regions of different potentials for elevated indoor radon concentration. For water
supplies in areas of low indoor air radon potential, it will be difficult to identify
and mitigate enough homes to achieve an equivalent or better health-risk reduc-
tion by treating the air. For such water supplies, it is unlikely that a public water
system’s multimedia mitigation program will be practical unless the water con-
centration of radon is only slightly above the MCL.

In areas of medium and high indoor air radon potential, it is more feasible to
mitigate a small number of high-indoor-concentration homes to provide an
equivalent health-risk reduction at a cost less than the cost of mitigating the
water. In this scenario, the public water supply would have to actively recruit
high-indoor-air radon concentration homes and mitigate them. Incentives could
perhaps be used to get participation of homeowners in these multimedia pro-
grams. In addition, the utilities would have to monitor and maintain the air
mitigation systems routinely. This scenario would require water utilities to be-
come involved in air mitigation in individual homes, something with which they
are likely to have little experience.

Reduction of radon in indoor air can be an alternative means of reducing
overall risks associated with radon. One way to achieve this is to install active
(mechanical) systems to reduce radon entry into existing or new houses. Ad-
equate testing (long-term measurements in the living space to reflect actual expo-
sures) will be necessary to determine which existing houses should be mitigated.
Routine follow-up measurements will be needed, both to determine the risk re-
duction achieved by the mitigation and to ensure continued successful operation
of the mitigation systems. To ensure that health-risk reductions are at least as
great as the reductions that would result from reducing the water radon concen-
tration to the MCL, the number of homes with air mitigation systems should be
10-20% greater than the calculated minimum number of homes. Radon-resistant
new construction methods could also be used although the technical and practical
bases of their implementation are still poorly developed. Evaluation of the base-
line radon exposure would require use of radon-monitoring data from existing
houses in the community of interest or estimates of average indoor concentrations
based on calculated radon potentials for the region. Careful attention to the fol-
low-up monitoring results would be important, both for determining how much
radon reduction has resulted (on the basis of aggregate comparisons) and for
determining whether radon persists at unacceptable concentrations.

Various educational and outreach programs reviewed by this committee in-
dicate that, in general, public apathy about the potential risks of exposure to


radon has generally remained, despite numerous and sometimes costly public
education efforts. Though the evaluation of many of these programs has not been
rigorous, on the basis of the reported results, the committee concludes that an
education and outreach program would be insufficient to provide a scientifi-
cally sound basis for claiming equivalent health-risk reductions and that an
active program of mitigation of homes would be needed to demonstrate
health-risk reduction.

Furthermore, the mitigation of indoor-air radon concentrations in a small
number of homes means risk reduction among only a few people who had high
initial risk, rather than uniform risk reduction for a whole population served by
the water utility. This approach raises questions of equity among the various
groups that are being exposed to various levels of risk associated with radon.
Equity issues would also result if the airborne-radon risks in one community were
traded for the risks in another without a resulting identical or improved public
health effect and a commensurate economic benefit to both communities. Non-
economic considerations could play a large role in the evaluation of multime-
dia mitigation programs and might be the deciding factors in whether to
undertake such a program. In any planning process, a careful program of
public education, utilizing experts in risk communication, will be essential to
give the public an adequate perspective of the tradeoffs in risks being proposed
and of the health and economic costs and benefits that will be produced by the
various alternatives.

EPA and the state agencies responsible for water quality will continue to be
faced with the problem of the health risks associated with the presence of radon in
drinking water. The increment in indoor radon that emanates from the water will
generally be small compared with the average concentration of radon already
present in the dwellings from other sources. Thus, except in situations where
concentrations of radon in water are very high, the reduction of radon in water
will generally not make a substantial reduction in the total radon-related health
risks to occupants of dwellings served by the water supply. However, the risks
associated with the waterborne radon are large in comparison with other regu-
lated contaminants in drinking water. Using mitigation of airborne radon to
achieve equivalent or greater health-risk reductions therefore makes good sense
from a public-health perspective. However, there are concerns that the equity
issues associated with the multimedia approach and other related issues will
become important in obtaining agreement by all of the stakeholders. This issue
will require each public water supply and the regulatory agency overseeing it to
study the circumstances carefully before deciding to implement a multimedia
mitigation program in lieu of water treatment.



Naturally occurring radioactivity can be found throughout the earth’s crust.
Some of these radionuclides decay into stable elements, such as 40K → 40Ar,
14C → 14N and 87Rb → 87Sr. Others are members of sequences of radioactive
decay in which one radionuclide decays into another radionuclide. The three
principal such series found in nature originate with 238U, 235U, and 232Th (NCRP
The immediate disposition of an atom created in a radioactive series depends
on physical and chemical properties of the element and on the surrounding soil or
rocks. Many of the elements in the process are metals such as uranium, thorium,
polonium, lead, and bismuth or alkaline earths such as radium. These elements
vary greatly in solubility depending on ambient physical and chemical conditions
and may go into solution or be absorbed onto organic particles or clay minerals.
Uranium, radium, and radon are the most mobile, lead and bismuth are only
moderately mobile, while thorium and polonium remain relatively immobile.
One of the most abundant sources of naturally occurring radioactivity is the
series that begins with 238U, which is illustrated in figure 1.1. The first 14 mem-
bers in this series collectively emit gamma, beta, and alpha radiation. Because of
the arrangement of half-lives and chemical properties, the concentration of radio-
activity of the early members of the series is proportional to the concentration of
238U in the earth.
An important deviation happens roughly midway through the 238U series:
226Ra decays by alpha emission, thereby creating 222Rn. In contrast with other



FIGURE 1.1 Decay scheme for natural occurring 238U chain.
members of the series, which are solids, radon is a chemically-inert noble gas and
can migrate in the environment.

A radon atom that is created deep within a grain of rock usually remains
there until it decays. However, when a radon atom is created near the surface of
a grain, it can recoil into the pore between grains; such radon atoms do not attach
or bind to the matrix that contains the immediate precursor, radium. The amount
of radon that reaches the pores is described by the emanation fraction. For typical
soils or bedrock, the emanation fraction can range from 5% to 50% (see the
review in Nazaroff 1992).
In most situations, the pore between grains of material contains a mixture of
air and water. Often, a recoil radon atom will come to rest in the water and remain


there (Tanner 1980). In addition to this direct process, a gas is partitioned be-
tween the air and water in the pore. This partitioning is described by Henry’s law
in terms of the Oswald coefficient, K:

K = Cw (1.1)

where Cw and Ca are the radon concentrations by volume (Bq m–3) in the water
and air, respectively. The Oswald coefficient varies inversely with temperature.
At 10 °C, KRn = 0.3; it increases to about 0.5 near 0 °C (Lewis and others 1987).
If the soil or bedrock is completely saturated with water, all the available radon
will be dissolved in the water.

Migration of radon in soil gas is controlled by two processes: molecular
diffusion and advective flow. Diffusion is the process whereby molecules mi-
grate toward regions with lower concentrations. Radon concentrations in soil gas
are typically 40,000 Bq m–3 and concentrations 10 to 100 times this value are not
uncommon. The main reason for this is that the radon atoms are confined within
a small volume defined by the pore space between the soil grains. Thus, radon
will preferentially diffuse toward regions that have lower concentrations, such as
caves, tunnels, buildings, and the atmosphere.

Advective flow is controlled by pressure differences. Air will flow toward
locations with lower pressure, and changes in atmospheric pressure can force air
into or out of the ground. Very often, the air inside a building is warmer than air
in the soil that is in contact with the building. This temperature difference causes
a pressure gradient that draws air containing high concentrations of radon into the
structure. Wind—as well as airflow from a fan, furnace, or fireplace—can also
reduce pressures inside a building, compared with the pressures in the soil adja-
cent to the building foundation. These processes constitute the primary reason
that radon enters and may be present in buildings at higher concentrations than in
ambient air.

The water supply can also contribute to indoor radon. When water leaves a
faucet, dissolved gases are released. This process is increased by mechanical
sprays during a shower or by the heating and agitation that occur during launder-
ing, washing, and cooking. The increase in the indoor radon concentration due to
radon release from indoor water use is described by the transfer coefficient:

T = ∆Ca (1.2)

where (∆––C–a) is the average increase of the indoor radon concentr–ation that results
from using water having an average radon concentration of CW. The various

sources of radon and the resulting radiation exposure pathways are shown in

figure 1.2.


FIGURE 1.2 Sources of radon and related radiation exposure pathways.
*Gamma exposure from radon collected during some mitigation procedures (see Appen-
dix E).

The first four descendants of radon—218Po, 214Pb, 214Bi, and 214Po—are also
radioactive and are collectively referred to as radon decay products. They are all
metals and have half-lives ranging from a fraction of a second to 27 min (see
figure 1.1). Indoors, some of these decay products come into contact with sur-
faces and are removed from the air by a process called plate-out. The rest of the
decay products remain suspended in air as free atoms (unattached) or combined
with other aerosols (attached). Although it is possible to measure the concentra-
tion of each radon decay product suspended in air, they are generally grouped. In
addition, the concentration is not presented in terms of activity per unit volume
(becquerel per cubic meter), but rather in terms of the total energy that would be
released by alpha particles when all the short-lived atoms decayed completely.
This quantity is called potential alpha energy (PAE), and the concentration in air


(PAEC), is measured in units of energy per unit volume of air (joules per cubic
meter (J m–3).

The development of a PAEC from indoor radon concentration depends on air
movement and aerosol conditions within a room. PAEC can depend on whether
the radon entered a room from soil or from water during bathing. The relationship
between indoor radon concentration and PAEC is expressed in terms of the
equilibrium ratio (ER). For a room without any depletion of radon or plate-out of
decay products, ER = 1.0. In domestic environments, ER ranges from 0.3 to 0.7
with a nominal value of 0.4 (Hopke and others 1995a).

The alpha-particle dose to lung tissues depends on PAEC and on the time
that a person spends in a given location. A combination of PAEC and time is a
measure of exposure expressed in joule-seconds per cubic meter (J. s m–3).


A person in a room will inhale radon decay products that are suspended in
air. Some activity can deposit and accumulate in the respiratory airways, de-
pending on breathing patterns and the aerodynamic size of the particles with
which the decay products are associated. Because of the short half-lives, the
radon decay products that are deposited in the lung will almost certainly decay
completely in the lung. The radiations emitted within the lung during these
decays can deposit energy in the body. However, this radioactivity is very near
the lung epithelium, so alpha particles in particular can transfer copious amounts
of energy to vulnerable cells. That is why radon decay products are character-
ized in terms of PAEC.

Radon gas itself is also inhaled. Most of it is exhaled immediately and
therefore does not accumulate in the respiratory system, as do radon decay prod-
ucts. Because the radon does not get close to radiosensitive cells, the absorbed
dose from alpha particles is small. However, some of the radon that reaches the
interior region of the lung is transferred to blood and dispersed throughout the
body. Radon and the decay products formed inside the body can deliver a radia-
tion dose to tissues and organs.

On some occasions, water is consumed immediately after leaving the faucet
before its radon is released into the air. This water goes directly to the stomach.
Before the ingested water leaves the stomach, some of the dissolved radon can
diffuse into and through the stomach wall. During that process, the radon passes
next to stem or progenitor cells that are radiosensitive. These cells can receive a
radiation dose from alpha particles emitted by radon and decay products that are
created in the stomach wall. After passing through the wall, radon and decay
products are absorbed in blood and transported throughout the body, where they
can deliver a dose to other organs.

Ingested water eventually passes through the stomach into the small intes-
tine, where the remaining radon and decay products are released from the water


and transferred to blood. They then circulate within the body; most are released
from the blood into the lung and exhaled, but some remain in the blood and
accumulate in organs and tissues, which receive an absorbed dose from alpha,
beta, and gamma radiation.


There is a direct implication between high doses of radiation and health
effects in humans. For example, excess cancers have been observed in a cohort of
survivors of the atomic-bomb blasts in Japan (National Research Council 1990a).
A relationship between lung cancer and inhalation of radon decay products has
been demonstrated in underground miners (Lubin and Boice 1997). Recent epi-
demiologic evidence suggests that inhalation of radon decay products in domes-
tic environments could also be a cause of lung cancer (National Research Council
1999; Lubin and others 1995). Although the studies do not specifically identify
health effects at low doses, there is compelling circumstantial evidence that they

Under ambient conditions of low dose and low dose rate, any health effects
associated with exposure to radon in air or water can be expected to occur from
the passage of single alpha particles through individual cells. Any given cell is hit
only once or not at all. An increase in exposure increases the number of cells that
are hit, but it will not affect the primary damage experienced by each cell. There-
fore, the initial events depend linearly on exposure or dose.

Exposed cells experience local damage in the form of DNA breaks and the
products of reactive oxygen. The damage is metabolized by cellular-repair sys-
tems, and some fraction of it results in permanent genetic changes. Those changes
can lead to the development of cancers; a cancer usually originates in a single
transformed cell.

Risk projection models have been developed to predict the risk in situations
where direct evidence is not available (National Research Council 1999; 1990a).
The nature of the exposure to indoor radon, the kinds of DNA damage inflicted
by alpha particles, and the extent of repair are consistent with the absence of a
threshold for cancer induction. The preferred model is a straight line that reaches
zero risk only when the dose or exposure is zero; it is referred to as the linear no-
threshold (LNT) model.


In 1988, Congress passed the Indoor Radon Abatement Act. Its stated goal
was to reduce indoor radon concentrations to outdoor levels. The Environmental
Protection Agency (EPA) was authorized to implement policies described in the
law. In 1987 and again in 1992, EPA published A Citizen’s Guide To Radon
(EPA 1992a). The document summarized the risks associated with inhalation of


radon decay products in residential environments. It recommended that people
measure indoor radon and consider taking action if the annual average concentra-
tion in their living areas exceeds 148 Bq m–3. EPA also developed programs in
support of its recommendations for mitigation (Page 1993): public-information
programs, a National Residential Radon Survey, Regional Radon Training Cen-
ters, the Radon Contractor Proficiency Program, the Radon Measurement Profi-
ciency Program, Radon Reduction in New Construction, and support for the
development of indoor-radon programs in individual states. As a result of those
efforts, about 11 million of the approximate 100 million single family dwellings
in the United States have been tested and about 300,000 (0.3%) mitigated in an
effort to reduce indoor radon concentrations (CRCPD 1994). In addition, EPA
estimates about 1.2 million new homes have been built with radon-resistant con-
struction methods (A. Schmidt, personal communication), although the success
of these methods is unknown.

It was recognized that water might also make a substantial contribution to
and in some circumstances be the primary source of health risks associated with
radon. In 1986, a revision to the Safe Drinking Water Act specifically required
EPA to set a standard for 222Rn in drinking water (US Congress 1986). After
litigation and a consent decree, EPA developed a criteria document that summa-
rized the health effects of radon and its prevalence in drinking water (EPA 1991a).
On the basis of the document and considerations of uncertainties in the analytic
procedures for testing for radon in drinking water, a regulation was proposed in
1991 that established a maximum contaminant level (MCL) of 11,000 Bq m–3
(EPA 1991b). That MCL corresponded to an lifetime individual health risk of
10–4 posed largely by an increase in radon in indoor air.

During the period permitted for public response after the announcement of
the proposed regulation, some groups supported reducing the MCL below
11,000 Bq m–3 because there is no known threshold for radiation-induced car-
cinogenesis. Others suggested raising the MCL because the increment in indoor-
air radon from water radon at 11,000 Bq m–3 would be about 2% of the annual
average residential radon concentration. There was also concern regarding the
dosimetry model used to estimate the risk of stomach cancer associated with
radon ingestion (Harley and Robbins 1994). As a result of those concerns, Con-
gress intervened in 1992 and directed the administrator of EPA to prepare a
multimedia risk assessment and cost estimates for compliance with regulations
regarding radon in drinking water. The reanalysis resulted in EPA’s revising its
risk assessment for the ingestion of water containing radon. As a result, the
ingestion risk and the inhalation risks (per unit of radon in drinking water) were
estimated to be about equal (EPA 1994b). This document was reviewed by the
Science Advisory Board (SAB) of EPA.

There was continuing concern about the estimates of stomach cancer result-
ing from radon ingestion. In addition, the SAB committee questioned the pru-
dence of regulating a small increase in indoor radon from water without consid-


ering the larger reductions in risk that might be obtained by reducing radon
concentrations originating from soil gas (EPA-SAB 1993a).

The Safe Drinking Water Act was amended again in 1996 (US Congress
1996). The proposed national primary drinking-water regulation for radon was
withdrawn. Before proposing a new regulation for radon in water, EPA was in-
structed to ask the National Academy of Sciences to prepare a risk assessment for
radon in drinking water on the basis of the best science available. The assessment
was to consider each of the pathways associated with exposure to radon from
drinking water at concentrations and conditions likely to be experienced in residen-
tial environments. The Academy was also asked to prepare an assessment of health-
risk reductions that have been realized from various methods used to reduce radon
concentrations in indoor air to provide a basis for considering alternative or multi-
media mitigation schemes as opposed to mitigation of water alone.


The Committee on the Risk Assessment of Exposure to Drinking Water in
the National Research Council’s Board on Radiation Effects Research began
deliberations in July 1997. The specific tasks assigned to the committee were:

• To examine the development of radon risk assessments for both inhala-
tion of air and ingestion of water.

• To modify an existing risk model if it were deemed appropriate or de-

velop a new one if necessary.

• To review the scientific data and technical methods used to arrive at risk

coefficients for exposure to radon in water.

• To assess potential health-risk reductions associated with various mea-

sures to reduce radon concentrations in indoor air.

The final report was to include:

• Estimates of lung, stomach, and other potential cancer risks per unit con-

centration of radon in water.

• Assessment of whether health effects of radon in drinking water could be

estimated for various sub-populations at risk, such as infants, children, pregnant
women, smokers, elderly persons, and seriously ill persons.

• Examination of evidence for teratogenic and reproductive effects in men

and women due to radon in water.

• Estimates of the transfer coefficient that relates radon in water to radon in

indoor air.

• Population-weighted estimates of radon concentrations in ambient air.
• Estimates of increases in health risks that could result from methods used

to comply with regulations for radon in drinking water.


• Discussion of health-risk reductions obtained by encouraging people to

reduce radon concentrations in indoor air with methods already developed and
comparison of them with the risk reductions associated with mitigation of radon
in water.


Chapter 2 presents baseline data regarding concentrations of radon in water
and indoor air. It includes a discussion of radon concentrations measured in
outdoor air throughout the United States and an estimate of a national annual
average concentration of ambient radon.

Chapter 3 describes the transfer coefficient that expresses the increase in
indoor airborne radon in reference to the concentration of radon in water. It
includes a survey of measurements and theoretical considerations.

Chapter 4 discusses the dosimetry of ingested radon. It describes patterns of
consumption of water directly from the tap or faucet. The calculations make
extensive use of physiologically-based pharmacokinetic (PBPK) models that have
been developed for dosimetry of internal radioactivity. The chapter includes
computations of equivalent dose and risk to individual tissues and organs. A
special model was developed to estimate the concentration of radon and the
alpha-particle radiation dose produced by decay of radon and its decay products
occurring next to sensitive cells in the stomach wall.

Chapter 5 discusses the risk associated with inhalation of radon and radon
decay products. It includes a summary of the methods used to form risk-projec-
tion models that were developed by the National Research Council’s committees
on Biological Effects of Ionizing Radiation (BEIR).

Chapter 6 discusses the basic mechanisms that are believed to be responsible
for radiation-induced carcinogenesis.

Chapter 7 presents an analysis of the uncertainty and precision associated
with the risk estimates obtained in the previous chapters.

Chapter 8 discusses the methods and efficiencies of radon mitigation in both
indoor air and water. It includes an examination of techniques for reducing radon
concentrations in existing buildings and procedures for reducing radon in new

Chapter 9 analyzes the concepts associated with a multimedia approach to
risk reduction. Several scenarios illustrate various ways to evaluate gains in risk
reduction by using an alternative AMCL for water with other indirect approaches
that encourage or even enforce mitigation in indoor air.

The committee’s research recommendations are summarized in chapter 10.
A glossary and six appendixes present specific details and methods that were
incorporated in the various chapters.



Baseline Information on Indoor Radon and
Radon in Water in the United States

Several databases provide a national picture of indoor radon and radon in
water for the United States. We provide these data here as context for the dis-
cussions in later chapters on ambient radon, transfer factors, uncertainty, mitiga-
tion, and a multimedia approach to risk reduction. Figure 2.1 is a geologic-
physiographic map of the United States that will serve as a general reference for
areas of the country that are important as sources of radon (Schumann and others
1994); it is derived from standard geologic and physiographic maps.

The concept of radon potential can be used as a basis for estimating indoor
radon concentrations. Although it is not possible to accurately predict radon
concentrations in individual houses because of the highly variable nature of
factors that control radon entry and concentrations in a specific house, one can
estimate the distribution of indoor radon concentrations on a regional basis. Sev-
eral approaches have been taken to develop indoor-radon potential maps of the
United States, and succeeding studies have built on previous ones; the most
recent maps of predicted indoor radon encompass a statistical analysis of vari-
ables that account for the greatest variation in indoor radon: geology, climate, and
house structure.
Figure 2.2 shows the geologic-radon potential map of the United States
developed by the US Geological Survey (Gundersen and others 1992) on the
basis of geology, indoor radon measurements, the aerial radiometric data col-
lected by the National Uranium Resource Evaluation (summarized in Duval and



FIGURE 2.1 Geologic-physiographic map of the United States (courtesy of USGS).

others 1989), soil permeability, and foundation housing characteristics. It is a
map of the land potential, not a map of exposure or risk. It was compiled from
individual state geologic-radon potential maps (Gundersen and others 1993) that
served as the basis of the Environmental Protection Agency (EPA) map of radon
zones that has been incorporated into one of the national building codes (EPA

Figure 2.3 shows the most recent and most comprehensive map of indoor-
radon potential and represents a prediction of the geometric mean of annual
exposure to indoor radon. The elements used in the map include the radium
content of the surficial soil derived from the aerial radiometric data collected by
the National Uranium Resource Evaluation (summarized in Duval and others
1989), information on the geologic province that comprises most of the county
(from the US Geological Survey), soil characteristics, the fraction of homes with
basements and with living-area basements, and radon-concentration surveys con-
ducted nationally and in each state from EPA and other sources. Those elements
are used in a Bayesian mixed-effects regression model to provide predictions of
the geometric mean indoor radon concentration by county. Additional details of
the model are given in Price (1997). The predicted county means have standard
errors of 15-30% for typical counties; the uncertainty in a given county depends
on the number of radon measurements in the county and the level of detail in the
geologic information.


FIGURE 2.2 Geologic-radon potential map of the United States (Courtesy of USGS).

FIGURE 2.3 Indoor-radon potential [predicted geometric mean air concentration in living area, Bq/m3]. 35


From figures 2.2 and 2.3, it is obvious that the Appalachian Mountains,Figure2.3Indoorrdon otentil[redictedgeometricmen irconcentr3ti]o.ninl
Rocky Mountains, Colorado Plateau, and northern glaciated states (states north
of the limit of glaciation) tend to have the highest radon potential and indoor
radon. The principal geologic sources of radon in the United States are:

• Uranium-bearing metamorphosed rocks, volcanics, and granite intrusive

rocks that can be highly deformed or sheared (shear zones in these rocks cause
the largest indoor-radon problems in the United States), found predominantly in
the Appalachian Mountains, Rocky Mountains, and Basin and Range;

• Glacial deposits derived from uranium-bearing rocks and sediments found

in the northern tier of states above the limit of glaciation;

• Marine black shales found in the Appalachian Plateau and Great Plains

and to a smaller extent in the Coastal Plain, Colorado Plateau, and Basin and

• High-iron soils derived from carbonate, especially in karstic terrain found

in the Appalachian Plateau, Appalachian Mountains, and Coastal Plain; and

• Uranium-bearing fluvial, deltaic, marine, and lacustrine deposits and phos-

phatic deposits found in the Colorado Plateau, Rocky Mountains, Great Plains,
Coastal Plain, Basin and Range, and Appalachian Plateau.


In the 1980s, a number of national studies of radon and other radionuclides in
public water supplies and groundwater in the United States were published (see
(Longtin 1988; Michel and Jordana 1987; Hess and others 1985; Horton 1983).
These studies examined geographic distribution, the controls of hydrogeology,
and differences among private well, small public, and large public water supplies.
The most common conclusions of the studies suggest that the highest radon
concentrations in groundwater and public water supplies generally occur in por-
tions of the Appalachian Mountains, Rocky Mountains, and Basin and Range.
Private well sources and small public water supplies tend to be higher in radon
than large public water supplies. Private well sources and small water supplies
tend to be in aquifers with low capacity. When these types of aquifers are ura-
nium bearing granite, metamorphic rocks, or fault zones (as found in the moun-
tain states), the radon concentration in the water tends to be high. Large public
water supplies tend to use high-capacity sand and gravel aquifers, which gener-
ally comprise low-uranium rocks and sediments and tend to be lower in radon.

The study of Hess and others (1985) examined 9,000 measurements of radon
in water from national and state surveys. Data were compiled for all but 10 states.
Public water supplies originating in surface water tended to have radon concen-
trations less than 4,000 Bq m–3. Private water supplies were higher in radon than
public water supplies by factors of 3 to 20. States with the highest radon in private
well water were Rhode Island, Florida, Maine, South Dakota, Montana, and

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